Functional activation by glucagon of glucose 6‐phosphatase and gluconeogenesis in the perfused liver of the fetal guinea pig

Band, Geoffrey C.; Jones, C. T.

doi:10.1016/0014-5793(80)81028-3

Cited by 21 publications

(12 citation statements)

References 18 publications

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“…The modulatory effect of glucagon on pyruvate kinase accounts for the down-regulation of glycolysis (9) . Glucagon also regulates glycogen synthesis and lysis by modulating the activity of glycogen synthase and glycogen phosphorylase via the phosphorylation of these enzymes (113) . Glucagon is not only implicated in glucose homeostasis but in hepatic lipid metabolism as well.…”

Section: Effects Of Glucagon On Hepatic Nutrient Metabolismmentioning

confidence: 99%

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

et al. 2014

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Glucose homeostasis is precisely regulated by glucagon and insulin, which are released by pancreatic a-and b-cells, respectively. While b-cells have been the focus of intense research, less is known about a-cell function and the actions of glucagon. In recent years, the study of this endocrine cell type has experienced a renewed drive. The present review contains a summary of established concepts as well as new information about the regulation of a-cells by glucose, amino acids, fatty acids and other nutrients, focusing especially on glucagon release, glucagon synthesis and a-cell survival. We have also discussed the role of glucagon in glucose homeostasis and in energy and lipid metabolism as well as its potential as a modulator of food intake and body weight. In addition to the well-established action on the liver, we discuss the effects of glucagon in other organs, where the glucagon receptor is expressed. These tissues include the heart, kidneys, adipose tissue, brain, small intestine and the gustatory epithelium. Alterations in a-cell function and abnormal glucagon concentrations are present in diabetes and are thought to aggravate the hyperglycaemic state of diabetic patients. In this respect, several experimental approaches in diabetic models have shown important beneficial results in improving hyperglycaemia after the modulation of glucagon secretion or action. Moreover, glucagon receptor agonism has also been used as a therapeutic strategy to treat obesity.

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Section: Effects Of Glucagon On Hepatic Nutrient Metabolismmentioning

confidence: 99%

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

et al. 2014

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“…G-6-P is then converted into glucose by glucose-6-phosphatase (G-6-Pase), increasing the glucose pool for hepatic output (47,50). In addition to activating the PKA-glycogen phosphorylase kinaseglycogen phosphorylase cascade, glucagon has been shown to increase G-6-Pase activity (3,4,82). Recent studies suggest that the upregulation of G-6-Pase by glucagon is at least partially due to increased transcription of the G-6-Pase gene in a PKA-dependent fashion involving peroxisome proliferator-activated re-ceptor-␥ coactivator-1 (PGC-1), a nuclear transcriptional factor coactivator (95).…”

Section: Molecular Mechanism For Glucagon-mediated Glucose Regulationmentioning

confidence: 99%

Glucagon and regulation of glucose metabolism

Jiang

Zhang

2003

American Journal of Physiology-Endocrinology and Metabolism

715

562

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As a counterregulatory hormone for insulin, glucagon plays a critical role in maintaining glucose homeostasis in vivo in both animals and humans. To increase blood glucose, glucagon promotes hepatic glucose output by increasing glycogenolysis and gluconeogenesis and by decreasing glycogenesis and glycolysis in a concerted fashion via multiple mechanisms. Compared with healthy subjects, diabetic patients and animals have abnormal secretion of not only insulin but also glucagon. Hyperglucagonemia and altered insulin-to-glucagon ratios play important roles in initiating and maintaining pathological hyperglycemic states. Not surprisingly, glucagon and glucagon receptor have been pursued extensively in recent years as potential targets for the therapeutic treatment of diabetes.

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“…Lipolysis releases glycerol from adipose tissues, which is a substrate for the production of glucose in the liver. In addition, accumulated cAMP induced by glucagon stimulates the expression of the genes for the key gluconeogenic enzymes PEPCK and glucose‐6‐phosphatase (G6Pase) (Band and Jones, 1980a, 1980b; Beale et al, 1984; Striffler et al, 1984; Iynedjian et al, 1985; Christ et al, 1988; Yoon et al, 2001) and suppresses expression of the genes for the key enzyme of the glucolytic pathway, namely, pyruvate kinase (Pilkis and Claus, 1991). As a result, it stimulates gluconeogenesis in the liver.…”

Section: Indirect Autonomic Nerve Pathways Regulating Hepatic Functionmentioning

confidence: 99%

Neural connections between the hypothalamus and the liver

2004

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After receiving information from afferent nerves, the hypothalamus sends signals to peripheral organs, including the liver, to keep homeostasis. There are two ways for the hypothalamus to signal to the peripheral organs: by stimulating the autonomic nerves and by releasing hormones from the pituitary gland. In order to reveal the involvement of the autonomic nervous system in liver function, we focus in this study on autonomic nerves and neuroendocrine connections between the hypothalamus and the liver. The hypothalamus consists of three major areas: lateral, medial, and periventricular. Each area has some nuclei. There are two important nuclei and one area in the hypothalamus that send out the neural autonomic information to the peripheral organs: the ventromedial hypothalamic nucleus (VMH) in the medial area, the lateral hypothalamic area (LHA), and the periventricular hypothalamic nucleus (PVN) in the periventricular area. VMH sends sympathetic signals to the liver via the celiac ganglia, the LHA sends parasympathetic signals to the liver via the vagal nerve, and the PVN integrates information from other areas of the hypothalamus and sends both autonomic signals to the liver. As for the afferent nerves, there are two pathways: a vagal afferent and a dorsal afferent nerve pathway. Vagal afferent nerves are thought to play a role as sensors in the peripheral organs and to send signals to the brain, including the hypothalamus, via nodosa ganglia of the vagal nerve. On the other hand, dorsal afferent nerves are primary sensory nerves that send signals to the brain via lower thoracic dorsal root ganglia. In the liver, many nerves contain classical neurotransmitters (noradrenaline and acetylcholine) and neuropeptides (substance P, calcitonin gene-related peptide, neuropeptide Y, vasoactive intestinal polypeptide, somatostatin, glucagon, glucagon-like peptide, neurotensin, serotonin, and galanin). Their distribution in the liver is species-dependent. Some of these nerves are thought to be involved in the regulation of hepatic function as well as of hemodynamics. In addition to direct neural connections, the hypothalamus can affect metabolic functions by neuroendocrine connections: the hypothalamus-pancreas axis, the hypothalamus-adrenal axis, and the hypothalamus-pituitary axis. In the hypothalamus-pancreas axis, autonomic nerves release glucagon and insulin, which directly enter the liver and affect liver metabolism. In the hypothalamus-adrenal axis, autonomic nerves release catecholamines such as adrenaline and noradrenaline from the adrenal medulla, which also affects liver metabolism. In the hypothalamuspituitary axis, release of glucocorticoids and thyroid hormones is stimulated by pituitary hormones. Both groups of hormones modulate hepatic metabolism. Taken together, the hypothalamus controls liver functions by neural and neuroendocrine connections.

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Functional activation by glucagon of glucose 6‐phosphatase and gluconeogenesis in the perfused liver of the fetal guinea pig

Cited by 21 publications

References 18 publications

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

Nutrient regulation of glucagon secretion: involvement in metabolism and diabetes

Glucagon and regulation of glucose metabolism

Neural connections between the hypothalamus and the liver

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